Nck2 vs. wt morpholino
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE1894 | GEO | 2004/10/30
SECONDARY ACCESSION(S): PRJNA90979
REPOSITORIES: GEO
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Project description:pooled individuals of nck2 and control morpholinos are compared in duplicated (A and B) hybridisations
2008-06-11 | E-GEOD-1894 | biostudies-arrayexpress
Project description:TÜAB zebrafish were maintained at 28.5 °C in in 1x Danieau solution (58 mM NaCl, 0.7 mM KCl, 0.4 mM MgSO4, 0.6 mM Ca (NO3)2, 5 mM HEPES, pH 7.6, 0.0001 % Methylene blue). Morpholinos (Gene Tools, Philomath, OR) were designed against Danio rerio lin-9 homolog (Genebank accession NM_001044946). The morpholino (MO) sequences were MO-E1 5´-GTTAGTTTTATTACTCACTCTCGTC-3´ and 5-base mismatch morpholino MO-E1mis 5´-GTTACTTTTAATACTGACTGTCCTC-3´. 7 ng of morpholinos were injected into one cell-stage embryos. 20 embryos per condition (MO E1; MO E1mis) were pooled for RNA purification 24 h post fertilization. Using the two color Quick-Amp Labeling Kit (Agilent; 5190-0444) 100 ng of total RNA were used for cDNA synthesis, mRNA amplification and labeling according to manufacturers instructions. Transcriptional profiling was done on a zebrafish oligo array (Agilent; G2519F AMADID 019161) in a 4 x 44K slide format and analyzed as described before.<br>
2009-03-28 | E-MEXP-2100 | biostudies-arrayexpress
Project description:Comparison of pooled Dll1tm1Gos and wildtype E10.5 embryo samples. 4 dual-color DNA-chip hybridizations on a non-commercial cDNA chip and 9 dual-color hybridisations on a commercial chip (Atlas Glass Mouse 1) of cDNAs from a pool of embryos were made. Keywords: other
2005-03-01 | GSE2273 | GEO
Project description:Background: Maintenance of the kidney filtration barrier requires coordinated interactions between podocytes and the underlying glomerular basement membrane (GBM). GBM ligands bind podocyte integrins to trigger actin-based signaling events critical for adhesion. Nck1/2 adaptors have emerged as essential regulators of podocyte cytoskeletal dynamics. However, the precise signaling mechanisms mediated by Nck1/2 in podocytes remain to be fully elucidated. Methods: We generated podocytes deficient in Nck1 and Nck2, and used transcriptomic approaches to profile expression differences. We further applied proteomic techniques to identify specific binding partners for Nck1 and Nck2 in podocytes. We used cultured podocytes and mice deficient in Nck1 and/or Nck2 along with podocyte injury models to comprehensively verify our findings. Results: Compound loss of Nck1/2 resulted in altered expression of genes involved in actin binding, cell adhesion and extracellular matrix composition. Accordingly, Nck1/2-deficient podocytes showed defects in actin organization and cell adhesion in vitro, with podocyte detachment and altered GBM morphology present in vivo. We identified distinct interactomes for Nck1 and Nck2, and uncovered a mechanism by which Nck1 and Nck2 cooperate to regulate actin bundling and integrin activation at focal adhesions via α-actinin-4. Furthermore, we found that loss of either Nck1 or Nck2 resulted in increased matrix deposition in vivo, with more prominent defects in Nck2 deficient mice, consistent with enhanced susceptibility to podocyte injury. Conclusion: These findings highlight distinct yet complementary roles for Nck proteins in regulating podocyte adhesion, controlling GBM composition and sustaining filtration barrier integrity.
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Project description:Chromatin immunopurifications from heat shocked drosophila embryos with anti-Heat shock factor sera compared with immunopurification with pre-immune sera. Hybridisations to cDNA arrays. Keywords: repeat sample
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Project description:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2α-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders. Differential gene expression profile between epididymal white adipose tissue of Nck2-/- and Nck2+/+ mice by RNA sequencing (Illumina HiSEq 2000)
2016-07-01 | E-GEOD-63510 | biostudies-arrayexpress
Project description:We used morpholinos and gene editing tools to inactivate the srsf5a gene. In contrast to srsf5a homozygous mutants that did not display any phenotypic traits, microinjection of sMOsrsf5a led to developmental defects. By using RNA sequencing on morphants and control embryos we were able to identify a plethora of morpholino inadvertant target.
2018-02-22 | GSE98888 | GEO
Project description:This dataset provides gene expression levels of single cell and pooled embryos as part of a study on zygotic genome activation in Ciona embryogenesis. The single cell RNA-seq data suggested that Cyclin B3 was a key mediator of this process. This was confirmed by performing RNA-seq on pooled RNA isolated from embryos where Cyclin B3 was knocked down (using morpholinos) or overexpressed (using mRNA injections).
2018-07-06 | GSE110588 | GEO
Project description:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2α-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders.
2016-07-01 | GSE63510 | GEO
Project description:Every individual (W1-W4) was hybridised 4 times, including 2 dye swaps: W1: 23573-23576; W2: 23577-23580; W3: 23581-23584; W4: 23585-23588. Only 2 of 4 hybridisations wer made at the same preparation Keywords: parallel sample
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